Previous studies indicate that complete loss of FUS could be sufficient to lead to FTD like symptoms in mice, and this was consistent with the role of FUS in controlling the splicing of mRNAs relevant to FTD, such as MAPT, encoding the TAU protein, or in the stability of mRNAs encoding relevant synaptic proteins such as GluA1 and SynGAP135–39. The gene discussed is GRIA1; the disease is frontotemporal dementia.